The authors reply.

e1014 www.ccmjournal.org October 2016 • Volume 44 • Number 10 Hatib et al (2) now report a similar case involving a 4-year-old boy, presenting with a supraventricular tachycardia. The child was intubated and received a bolus of amiodarone with a subsequent continuous infusion of 15 μg/kg/min into a femoral access line (triple lumen catheter) leading to sufficient rate control. When found to be intra-arterial, the drip was immediately stopped and the access removed. Clinical signs of arterial damage remained absent; however, vascular ultrasound was not performed and laboratory tests for ischemia, such as lactate, were not determined. The case by Hatib et al (2) is interesting and illustrates the risk of accidental intra-arterial cannulation in emergency settings. However, in this context, amiodarone did not appear to cause such serious harm as encountered in our case. Some distinct differences may be the reason for this notion. In our scenario, angiography revealed a local thrombus formation in the brachial artery, precisely where the amiodarone bolus had been administered. This led us to suspect regional endothelial damage as the underlying cause for thrombotic occlusion. The vascular cytotoxic effects of amiodarone are dose-dependent and well characterized (3). Several factors are of critical importance for the bioactivity of the drug at the vessel wall and directly correlate with its cytotoxicity: 1) the administered amount and local concentration of the drug, 2) which is determined by local blood flow, and 3) the size of the vessel.